Abstract

The effect of saralasin, a clinically employed angiotensin antagonist, upon hemodynamics and plasma catecholamine concentration was compared to the infusion of noradrenaline. These studies were carried out to determine if a transient pressor effect frequently observed during saralasin infusion might be mediated by release of catecholamines from the adrenal medulla. After five minutes of saralasin infusion, mean arterial pressure rose significantly, pulse rate fell slightly, and plasma noradrenaline increased by 115 +/- 28 pg./ml. Plasma adrenaline was unchanged. After 30 minutes of saralasin infusion, mean arterial pressure was at control levels and plasma catecholamine concentrations were also no different from pre-infusion levels. Infusion of noradrenaline produced a hemodynamic pattern similar to that observed during the first five minutes of saralasin infusion. However, there was a thirteen-fold increase of plasma noradrenaline observed when compared to the first five minutes of saralasin infusion. It was concluded that the transient pressor action of saralasin could not be explained by release of catecholamines from the adrenal medulla. However, the very slight increase in plasma norepinephrine observed during the first five minutes of saralasin infusion may imply altered function of sympathetic neurons.

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This record was last updated on 07/01/2016 and may not reflect the most current and accurate biomedical/scientific data available from NLM.
The corresponding record at NLM can be accessed at https://www.ncbi.nlm.nih.gov/pubmed/619593